Case Report Pulmonary Alveolar Microlithiasis and Rheumatoid Arthritis: A Case Report and Review of the Literature Waleed Hafiz , 1,2 Ahmedhusam Alahmed, 2 Mohammed Alahmadi, 1 Rakan Alotaibi, 1 Abdullah Alsharif, 1 Safwan Alim, 1 Mohammed Mokhtar, 1 Kholoud Al-Maabdi, 3 and Omaima Badr 2 1 Department of Medicine, College of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia 2 Department of Medicine, Alnoor Specialist Hospital, Makkah, Saudi Arabia 3 Department of Medicine, East Jeddah Hospital, Jeddah, Saudi Arabia Correspondence should be addressed to Waleed Hafiz; wahafiz@uqu.edu.sa Received 11 July 2020; Accepted 20 May 2021; Published 31 May 2021 Academic Editor: Tsai Ching Hsu Copyright © 2021 Waleed Hafiz et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pulmonary alveolar microlithiasis is a rare autosomal recessive condition that is characterized by the formation of excessive calcium phosphate microliths in the alveoli. Most patients are diagnosed in adulthood due to the slow progression of the disease. Children with this disease are asymptomatic, and changes in the lung parenchyma are usually discovered incidentally. e diagnosis is made by the combination of a positive chest imaging and histological examination. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by chronic seropositive symmetrical inflammatory polyarthritis with nu- merous extra-articular manifestations. It targets the lining of the synovial membranes, frequently affects females more than males, and is treated with the disease-modifying antirheumatic drugs (DMARDs). If left untreated, it leads to increased morbidity, mortality, and socioeconomic burdens. In this case, we report a 19-year-old young man who presented with clinical and ra- diographic features of PAM associated with RA. 1. Introduction Pulmonary alveolar microlithiasis (PAM) is a fairly rare lung disease which is characterized by the deposition of alveolar calcium and phosphate in the lung tissues bilaterally and predominantly affecting the lower and middle lung zones. e etiology and pathogenesis are not completely under- stood [1, 2]. PAM is a genetic disease caused by a mutation in the SLC34A2 gene. is gene is a sodium-dependent phosphate transporter expressed in the lungs which is essential in the removal of phospholipids from the alveolar spaces. Dys- functional SLC34A2 leads to the accumulation of calcium and phosphate causing microlithiasis [3]. PAM is considered an autosomal recessive disorder and is associated with consanguinity. A majority of patients have at least one affected sibling. Over 1200 cases were reported in the literature, and its prevalence is unknown. 35.8% of PAM patients are diagnosed before the age of 20 and 88.2% before the age of 55 [4]. In early stages, patients are asymptomatic with a usual slow progression. Over time, they develop exertional dyspnea, dry cough, weakness, chest pain, cyanosis, he- moptysis, and pneumothorax. Physical examination may show rales and bilateral clubbing of the finger. Additionally, it has been shown that smoking and infection may hasten the disease progress [4]. PAM is mainly diagnosed by imaging with the support of clinical manifestations. e typical findings of PAM on a plain radiograph are a fine scattered micronodular pattern forming a characteristic “sandstorm” sign. e borders of the heart, diaphragm, and vascular markings are obscured due to the dense calcification. Findings on the high-reso- lution computed tomography (HRCT) scan of the chest are Hindawi Case Reports in Rheumatology Volume 2021, Article ID 8811507, 4 pages https://doi.org/10.1155/2021/8811507